Is Deferoxamine a suitable therapy for Diabetes in patients with over 500 ng/mL Ferritin?

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Interactions between Iron load and Insulin sensitivity

Also, Fargion et al. (8) studied a cohort of 40 patients with hyperferritinemia and found IR in
69%. Several hypotheses have been postulated to explain this association. Iron overload is believed to lead to IR, as suggested by the fact that iron depletion can improve insulin sensitivity (9–11).
Also, a recent study showed a decrease in the development of diabetes mellitus in blood donors,
which correlated with a reduction in iron deposits and an increase in insulin sensitivity (12). Besides, iron overload can interfere with insulin signaling through the induction of reactive oxygen species, the latter impairing insulin uptake through a direct effect on insulin receptor function, by
inhibiting the translocation of GLUT4 to the plasma membrane (13, 14) and iron can also induce IR of glucose transport in adipocytes (15).Nash, insulin resistance and iron 2006

Association with hyperparathyroidism

In contrast to the novel work with PTHrP, parathyroid hormone (PTH) has a longstanding clinical link with CPPD deposition disease. Hyperparathyroidism is a well-established risk factor for chondrocalcinosis [25]. This year, Pawlotsky et al. [26•] demonstrated how this connection might be broadened to apply to hemochromatosis, another metabolic disorder associated with chondrocalcinosis. In this study, the authors hypothesized that the arthritis associated with hemochromatosis might be related to increased levels of PTH in these patients. They found that of the 210 patients with hemochromatosis tested, one third had elevated PTH 44-68 levels, and that levels of this PTH fragment correlated with serum ferritin and the number of affected joints. They postulated that this PTH fragment might affect mineralization of bone and cartilage. The authors propose that elevated levels of this PTH fragment may result from iron deposition in the parathyroid gland itself. Certainly, further studies are necessary to establish the connection between iron overload and increased serum PTH fragments. However, this work suggests at least one common thread between the seemingly heterogeneous group of metabolic abnormalities associated with CPPD deposition. It will be interesting to see if these PTH fragments have direct effects on articular cartilage, and whether these PTH fragments are elevated in patients with idiopathic CPPD deposition disease. FullText